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Effect of Selenium on Testicular Tissue in Adult NMRI Mice Following Cyclophosphamide-Induced Toxicity

Jul 2026 · Journal of Shahid Sadoughi University of Medical Sciences · 0 citations

TL;DR

It is shown that cyclophosphamide induces oxidative stress, causes disruption in the structure and function of the testis, and selenium reduced these damages and improved important histological and oxidative stress parameters to levels similar to the control group, suggesting a protective role against cyclophosphamide-induced testicular damage.

Abstract

Introduction: Cyclophosphamide, as a chemotherapeutic drug, causes induction of oxidative stress and disruption in the testis structure and function. In this study, the effect of selenium as a strong antioxidant on the testicular tissue of male mice after treatment with cyclophosphamide was evaluated. Methods: For this experimental study, 32 adult male NMRI mice were divided into four groups of eight: control, cyclophosphamide (100 mg/kg, administered once weekly), selenium (1 mg/kg daily for 35 days), and a combination of cyclophosphamide and selenium. Following the 35-day treatment period, the mice were dissected; the left testis was utilized to measure malondialdehyde (MDA) levels and total antioxidant capacity (TAC), while the right testis, after undergoing fixation, tissue processing, sectioning, and hematoxylin-eosin staining, was employed for stereological analyses. Data were analyzed using SPSS software, applying one-way ANOVA followed by Tukey’s post-hoc test, with statistical significance set at p<0.05. Results: In the cyclophosphamide group compared to control, a significant decrease was observed in mean total testis volume, seminiferous tubules volume (p<0.001), interstitial tissue volume (p<0.01), as well as in the length, diameter, and height of the germinal epithelium. basement membrane thickness, number of spermatogenic, Sertoli and Leydig cells, spermatogenesis indices, Johnsen score, and TAC level of testicular tissue (p<0.001), while the MDA level significantly increased (p<0.001). In the cyclophosphamide plus selenium group, these changes were compensated at the control level. Conclusion: The results showed that cyclophosphamide induces oxidative stress, causes disruption in the structure and function of the testis. While selenium reduced these damages and improved important histological and oxidative stress parameters to levels similar to the control group, suggesting a protective role against cyclophosphamide-induced testicular damage.

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